OBJECTIVE: Ameloblastoma and keratocystic odontogenic tumor (KOT) is characterized by a benign but locally invasive behavior with a high risk of recurrence. MDM2 (murine double minute 2), an amplifier of cell proliferation, and p53, a tumor suppressor gene, are overexpressed in some odontogenic lesions. The aim of this study was to compare the expression of MDM2 and p53 in ameloblastoma and KOT as 2 lesions with similar biologic behavior, by immunohistochemistry. METHODS: The expressions of MDM2 and p53 proteins were determined in 39 ameloblastomas (15 follicular types, 15 plexiform types, and 9 unicystic types) and 15 KOTs. RESULTS: P53 protein was expressed in 100% of KOTs and 77.8% of ameloblastomas, and MDM2 was detected in 74.8% of ameloblastomas and 80% of KOTs. There was no statistical difference between MDM2 and p53 expressions in different subtypes of ameloblastomas and also when KOTs were compared with them (P > 0.05). There was a significant difference between immunohistochemical reactivity of MDM2 among subtypes of ameloblastomas (P < 0.05). MDM2 and p53 expressions were positively correlated. CONCLUSIONS: Overexpression of p53 and MDM2 is associated with the pathogenesis and oncogenesis of ameloblastomas and KOT. Overexpression of these markers can contribute to similar biologic behavior of these lesions.
OBJECTIVE:Ameloblastoma and keratocystic odontogenic tumor (KOT) is characterized by a benign but locally invasive behavior with a high risk of recurrence. MDM2 (murine double minute 2), an amplifier of cell proliferation, and p53, a tumor suppressor gene, are overexpressed in some odontogenic lesions. The aim of this study was to compare the expression of MDM2 and p53 in ameloblastoma and KOT as 2 lesions with similar biologic behavior, by immunohistochemistry. METHODS: The expressions of MDM2 and p53 proteins were determined in 39 ameloblastomas (15 follicular types, 15 plexiform types, and 9 unicystic types) and 15 KOTs. RESULTS:P53 protein was expressed in 100% of KOTs and 77.8% of ameloblastomas, and MDM2 was detected in 74.8% of ameloblastomas and 80% of KOTs. There was no statistical difference between MDM2 and p53 expressions in different subtypes of ameloblastomas and also when KOTs were compared with them (P > 0.05). There was a significant difference between immunohistochemical reactivity of MDM2 among subtypes of ameloblastomas (P < 0.05). MDM2 and p53 expressions were positively correlated. CONCLUSIONS: Overexpression of p53 and MDM2 is associated with the pathogenesis and oncogenesis of ameloblastomas and KOT. Overexpression of these markers can contribute to similar biologic behavior of these lesions.